Tumor suppressor microRNAs are underrepresented in primary effusion lymphoma and Kaposi sarcoma

被引：80

作者：

O'Hara, Andrea J. ^{[1
]}

Wang, Ling ^{[1
]}

Dezube, Bruce J. ^{[2
]}

Harrington, William J., Jr. ^{[3
]}

Damania, Blossom ^{[1
]}

Dittmer, Dirk P. ^{[1
]}

机构：

[1] Univ N Carolina, Dept Microbiol & Immunol, Ctr AIDS Res, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

[2] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA

[3] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Viral Oncol Program, Coral Gables, FL 33124 USA

来源：

BLOOD | 2009年 / 113卷 / 23期

基金：

美国国家卫生研究院;

关键词：

ENDOTHELIAL-CELLS; PROLIFERATION; SURVIVAL; MIR-155; MIR-221; FAMILY; GROWTH; MYC;

D O I：

10.1182/blood-2008-09-179168

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The presence of tumor-specific microRNAs reflects tissue of origin and tumor stage. We show that the absence of miRNAs likewise can be used to determine tumor origin (miR-155) and proliferation state because tumor suppressor miRNAs (miR-222/221, let-7 family) were significantly down-regulated in primary effusion lymphoma (PEL) and in Kaposi sarcoma (KS), an endothelial cell tumor. PEL and KS are associated with KS-associated herpesvirus infection. We identified 15 virally regulated miRNAs in latently infected, nontumorigenic endothelial cells. MiR-143/145 were elevated only in KS tumors, not virally infected endothelial cells. Thus, they represent tumor-specific, rather than virus-specific, miRNAs. Because many tumor suppressor proteins are wild-type in KS and PEL, down-regulation of multiple tumor suppressor miRNAs provides a novel, alternative mechanism of transformation. (Blood. 2009; 113: 5938-5941)

引用

页码：5938 / 5941

页数：4

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